skimmed.cream.org Report : Visit Site


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    The main IP address: 80.87.134.99,Your server United Kingdom,London ISP:The Positive Internet Company Ltd  TLD:org CountryCode:GB

    The description :skimmed cream skimmed.cream.org menu skip to content cholesterol protective in elderly nature polarised emf nonsense search for: my unsurance policy fri 12th 2018f january 2018 general nickm i can oft...

    This report updates in 27-Sep-2018

Technical data of the skimmed.cream.org


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Latitude: 51.508529663086
Longitude: -0.12574000656605
Country: United Kingdom (GB)
City: London
Region: England
ISP: The Positive Internet Company Ltd

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ipv4:IP:80.87.134.99
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skimmed cream skimmed.cream.org menu skip to content cholesterol protective in elderly nature polarised emf nonsense search for: my unsurance policy fri 12th 2018f january 2018 general nickm i can often appear a cocky git, especially when discussing nutritional controversies; however, i try to entertain doubts as vehemently as i herald certainties. to keep myself honest, i must air these doubts, these areas where i cannot proclaim sure knowledge, whether through a fault in my own wisdom, a personal lack of understanding, or a true ambiguity in the field. so i present here my current “unsurance policy” against dunning kruger effectitis: how does hyperinsulinaemia hate? in metabolically enlightened circles, all the coolest kids finger insulin resistance (ir) as the root of the so-called diseases of civilisation. i have become increasingly convinced that we find not ir, per se, but hyperinsulinaemia itself, at the root of the problem. don’t blame the body for drawing up the drawbridges after a flood of insulin deluges each cell. blame the deluge. whatever your average blood glucose level, living a life marinaded in constant excess insulin devastates your healthful longevity, whether you’re a worm or a woman , a mouse or a man . whilst hyperglycaemia causes substantial harm, excess insulin causes many problems all on its own: the inflammatory responses, the anabolic state that encourages potentially mutagenic cell proliferation, as well as the general kick in the nuts to endocrine homoeostasis. but i still don’t enjoy a complete mechanistic understanding of exactly how having so much insulin in the body lies precisely at the feet of so many maladies. i would love someone to write a pop-sci book, using helpful analogies, beautiful illustrations and, if necessary, scratch-and-sniff stickers, that explains how excessive insulin really plays its part as the bad actor. at a cellular molecular level, what naughtiness lurks? and if, in fact, insulin lies upstream from that which actually does the in-situ damage, then i want to know all about it. protein, antitein? the pendulum of opinion about protein swings predictably – even tediously. a few years ago, we found jimmy moore suggesting that chomping down on protein had little to differentiate it from gorging on chocolate cake! more seriously, researchers like dr ron rosedale started reading the rosetta stone of the ancient mtor pathway and not liking the tale that emerged: excess protein, it suggested, encourages life’s candle to burn more quickly – the soma detects structural superfluity and energy abundance, so nature suggests one just breed and then bugger off. the way to longevity, then, requires us to eschew the whey. while the sugary carbaliers battled the fatty roundheads, they both batted about the “third” macronutrient, protein, as a pawn in the primary battle. and, yes, the pendulum has swung again. low carb doctors like ted naiman have adapted a kind of post-modern cico (however they protest that accusation). they proclaim that eating more protein and stopping your fat gluttony will help you lose weight and become generally healthier. mtor? meh-tor more like. beyond the swinging pendulum lie perennial questions, never conclusively answered, about how protein does or does not interfere with ketosis, and whether this matters, and how it does, or does not, promote additional gluconeogenesis to replace that ketotic deficit. for every person who claims additional protein as a silver bullet to satiety, another retorts that a protein glut shoots one in the fat-adapted foot, leading to ravenous annoyance. honestly, i don’t really know what to believe about this one. as a lover of biltong, i’d welcome it if ad-libitum protein had the blessings of my favourite gurus. but anyone who’s attended one of rosedale’s talks emerges certain that, at the very least, protein has a case to answer . perhaps a powerful one. does anyone have any convincing data here, one way or the other? let me know! carby conundrum? lchf works. we have the data. anyone who argues against it now as an effective strategy against hyperinsulinaemia thus makes an extraordinary claim, for which i demand extraordinary evidence to repudiate such an obviously successful methodology. of course, because the body relies largely on insulin signalling to process digestible carbohydrates, and because science agrees that those carbs have no essential role for humans, limiting their ingestion makes logical sense. we bolster that logic further when we realise our species went through a number of evolutionary funnels which demanded we thrive without any carbs. nevertheless, we do seem to find a few populations that survive, and perhaps even do well, on a higher carb diet. the blessed kitavans among them, perhaps. clearly, they have many factors at play. modern civilisation provides many more wonky paving-stones we can trip over than just a glut of exogenous glucose: air pollution, cocked-up circadian rhythms, even the stressful alienation from our evolved mores of socialisation. and, of course, the dreaded seed oils. so do the happy-yet-carby civilisations thrive because of the carbs, or despite them? have they inadvertently tipped the scales of health so profoundly that even a pile of insulin-spiking carbs can’t quite tip it askew the other way? or do their diets actively promote their healthful normo-insulinaemia? a few years ago, denise minger wrote a thought-provoking post about what she termed carbosis . if the magical realm of ketosis happens on a high-fat, low carb diet, then carbosis reflects its mirror image on a low-fat, high carb diet. whilst i disagree with some of her conclusions (it seems, for example, we might, fairly, call kempner a bit of a crook ), i still find much to intrigue me in her argument. i do believe that hyperinsulinaemia provides the key to unlocking much disease and disorder; so perhaps we can find not one, but two ways, to avoid turning that key: 1) lchf. eat food that doesn’t require much insulin intervention at all: namely, high fat food. avoid glycolytic foods that spike insulin in this regimen, because high fat foods reduce the cellular response to insulin (what some have termed “glucose sparing adaptation” or “benign physiological insulin resistance”). as such, any exogenous glucose causes a hyperglycaemic emergency in this context. 2) hclf: eat food that forces your body to use insulin efficiently: namely, high carb foods. avoid foods that induce glucose-sparing adaptation in this regimen (namely fats), to ensure that every cell listens carefully to insulin’s signal. the body needs to get the message that you provide glucose alone as its exogenous fuel. no mixed messages! both regimens, it seems, would result in a relatively low, and pulsatile, insulin pattern. i know which one i prefer, but perhaps a highly-restrictive hclf doesn’t simply tell a just-so story, but has some bearing in reality. if it does, then it still leaves unanswered to me some of the other problems one experiences when relying entirely on glycolysis: the age damage, the satiety deficit, the potential lack of ketogenic benefits. but we need convincing answers to these carby black cygnets that paddle about on our otherwise calm lchf pond. lipidy doo-dah? yes, the simple ancel keys lipid hypothesis has died. only anti-science organisations like the american heart association, or the british dietetic association, still try to animate the rotting corpse. the wonderful work by ivor cumins reveals how only a profoundly stupid – or myopic – person could rely on ldl-c or even ldl-p as a reliable causal marker of anything in particular. that said, i retain some tinges of concern. at some threshold, can the ldl particles themselves cause mischief all on their own, however much you’ve got the insulin beast under control? if so, who should worry about this? and how must they respond? since most data show that diets high in saturated fats do generally promote ld

URL analysis for skimmed.cream.org



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WHOIS LIMIT EXCEEDED - SEE WWW.PIR.ORG/WHOIS FOR DETAILS

  REFERRER http://www.pir.org/

  REGISTRAR Public Interest Registry

SERVERS

  SERVER org.whois-servers.net

  ARGS cream.org

  PORT 43

  TYPE domain

  REGISTERED unknown

DOMAIN

  NAME cream.org

NSERVER

  DNS1.POSITIVE-INTERNET.COM 80.87.136.65

  DNS0.POSITIVE-INTERNET.COM 80.87.128.65

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